Congenital Heart Disease I Flashcards

1
Q

What are the 5 congenital heart lesions that were talked about in the two congenital heart disease lectures? Which one is the most common?

A
  • Persistent ductus arteriosus (PDA)
  • Atrial Septal Defect (ASD)
  • Ventricular Septal Defect (VSD)
  • Tetralogy of Fallot (TOF)
  • Coarctation of the Aorta

PDA is the most common

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2
Q

What is a PDA and how does it form?

A

PDA is a shunt or a connection between the pulmonary artery and the aorta.

Usually stays patent because of prostaglandins. PGs keep these guys alive in the body.

Note: PDA in this case does not stand for Public Display of Affection which is also a condition that can affect the heart negatively.

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3
Q

How does the shunt work? What determines bloodflow?

A

Shunt direction is primarily determined by pressure or resistance difference between the 2 vessels it connects (true for any shunt in the body). Because aortic resistance and pressure are greater than pulmonary resistance and pressure blood shunts through PDA from aorta to pulmonary. this is an example of Left to Right shunt.

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4
Q

What is a left to right shunt?

A

blood flow from a systemic chamber into a pulmonary chamber

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5
Q

What are systemic chambers? What are pulmonary chambers?

A

systemic chambers: pulmonary veins, LA, LV, aorta

pulmonary chambers: systemic veins, RA, RV, pulmonary arteries

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6
Q

Clinical presentation of PDA?

A

can be asymptomatic if small. Big ones usually caught in neonates.

  • respiratory effects- increased work breathing. pulmonary edema/hemorrhage
  • hoarse cry
  • Other stuff that might occur if blood were going back into pulmonary artery from aorta: renal insufficiency (blood backup), CHF.
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7
Q

Physical exam findings with PDA?

A
  • wide pulse pressure (really low diastolic compared to systolic)
  • bounding pulses
  • machinery sounding murmur on upper L sternal border (this one is “classic” (i.e. important to know)).
  • accentuated P2 sounds if pulm. HTN present.
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8
Q

How to manage PDA?

A
asymptomatic= no worries
symptomatic= try meds first (cyclooxygenase inhibitors) then surgery if it doesn't work (ligation via lateral
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9
Q

Why do we use cox inhibitors with PDA? Which ones do we use

A

blocks conversion of arachadonic acid to prostaglandin. prostaglandins keeps the ductus patent.

indomethacin, ibuprofen, indocin, ibuprofen lysine (just to have read, probably not that important).

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10
Q

What complications do we see with PDA?

A
  • increased risk of subacute bacterial endocarditis.

- if large and untreated can result in veno-occlusive disease

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11
Q

What is ASD and how does it form (explain the embryology and what went wrong)?

A

atrial septal defect– there is a hole connecting the R and L atria.

Normally there is a big hole connecting the LA and RA called the ostium primum. The septum primum forms between the LA and RA and will close the ostium. As it closes a second hole forms in the septum primum called the ostium secundum. As this hole forms a second barrier forms to cover it up called the septum secundum. This hole is now the foramen ovale. After birth the flaps of the foramen (the septums) should close. In ASD they do not.

This is such a long notecard. Just go to slide 25 of her presentation if that didn’t help and figure it out there.

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12
Q

atrial septation occurs simultaneously with ______

A

ventricular septation

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13
Q

Which way willl blood generally travel in ASD? Why?

A

Generally it will travel from Left atrium to Right atrium.

blood flow direction depends on resistance to the LV because if the inflow path to the LV is harder than going to the RA, blood will flow from LA to RA.

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14
Q

key points of ASD clinical presentation.

A
  • rarely presents in infancy

- shunting increases as pulmonary vascular resistance falls and RV becomes more compliant.

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15
Q

Why do we hear a murmur with ASD?

A

we hear Systolic ejection murmur secondary to excessive bloodflow across the pulmonary valve. Also, will sometimes hear a diastolic murmur with excessive blood flow across tricuspid valves.

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16
Q

ASD can lead to RV volume overload and delayed RV emptying which can lead to what kind of heart sound?

A

widely split S2. The A2-P2 split of S2 also is more prominent than usual on inspiration. This is because the RV is being overloaded so there is delayed RV emptying. The S2 is split occurs in all phases of respiration.

This is a really good diagnostic tool–> ASD always have a S2 split.

17
Q

DIagnosis of ASD is usually done how?

A

Echocardiogram. see the defect and the magnitude of the shunt.

18
Q

What are the long term risks of hemodynamically significant ASD?

A
  • pulmonary vascular disease
  • atrial arrythmias
  • cardiac failure
19
Q

How do you manage ASD in infants? in older children and adults?

A

infants: meds can relieve symptoms- diuretics to relieve breathlessness. If infants are still symptomatic after meds see below.

older children: CLOSE THE HOLE! (surgery or percutaneous device closure)

20
Q

Summary Card
ASD

  1. Magnitude and direction of shunt depends on _______ and _________.
  2. ______ ventricle is more compliant than the _____ ventricle. This causes blood to shunt in what direction?
  3. Murmur is NOT caused by ________. Why?
  4. Murmur IS caused by _______.
  5. Embryologic basis of ASD is _______.
A
  1. size of defect, inflow resistance to RV vs LV
  2. Right; Left; L–>R flow
  3. flow across the defect. Pressure is too small
  4. excessive flow across the pulmonary valve (systolic) and tricuspid valve (diastolic)
  5. an excessive ostium secundum or an inadequate septum secundum.
21
Q

Whats the difference between PFO and ASD?

A

PFO (patent foramen ovale) won’t have any exam findings. PFO is a flap whereas ASD is an actual hole. PFO is just a variant of normal which doesn’t usually need to be fixed whereas ASD is a heart defect that can cause all sorts of stuff.

22
Q

What is the most common type of ASD?

A

ostium secundum ASD